Fat embolism syndrome
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  • 1. It is one of the causes of morbidity and mortality following # in patient with multiple injury  +  FES is an important cause of ARDS
  • 2.  Fat embolism syndrome is defined -- Post Traumatic Respiratory Distress Syndrome occurring within 72hrs of skeletal trauma  Earliest manifestations are -- Tachycardia -- Elevation of temperature above 38 deg -- falling PaO2
  • 3.  Fat embolism - this indicates presence of fat globules in lung parenchyma and peripheral circulation after fractures of long bones and other major trauma
  • 4. Fat embolism Syndrome-  A serious manifestation of the phenomenon of emboli resulting in a variety of symptoms
  • 5. Historical Review  In 1861, Zenker described fat droplets in the lung capillaries of a railroad worker who sustained a fatal thoracoabdominal crush injury.
  • 6.  In 1865, Wagner described the pathologic features of fat embolism.
  • 7. However, in 1873,Von Bergmann became the first to establish the clinical diagnosis of fat embolism syndrome.
  • 8. In a 38-year-old patient who sustained a comminuted fracture of the distal femur.  Postmortem examination revealed a large amount of pulmonary fat
  • 9.  Button – stated that 10% of battle casualities in World War 1 suffered from FES  World War 2 postmortem study revealed incidence of FES in 65% of patients.
  • 10. Causes  Traumatic  Non-traumatic
  • 11. Traumatic  # long bones  Multiple #s  surgical instrumentation of the medullary canal
  • 12. Non traumatic  Haemoglobinopahy  Collagen vascular disease  Diabetes mellitus  Severe infection  Neoplasm  Osteomyelitis  Blood transfusion  Cardiopulmonary bypass  Renal infarction  Decompression syndrome owing to altitude  Renal hemotransplantation
  • 13. Prevalence  Estimated to be 90% after major trauma  Clinical prevalence is said to range from .25% to 1.25%  Overall mortality is said to be between 10% and 20%
  • 14. Physiochemical theory of FES postulate Lipid profile instability after trauma Alteration in microcirculatory flow patterns Inadequate tissue perfusion Tissue hypoxia FES
  • 15. Pathophysiology Mechanical theory Biochemical theory
  • 16. Mechanical theory
  • 17. 1. Presence of torn blood vessels to permit fat to enter the circulation 2. Liberaration of free fat 1. A transient rise in marrow pressure above venous pressure to allow fat droplets to enter the circulation
  • 18. Biochemical theory  Toxic  Obstructive
  • 19. Toxic theory Lung lipase hydrolyses neutral fat to chemically toxic free fatty acids that cause severe inflammatory changes This causes severe inflammatory changes by producing endothelial damage ,inactivation of lung surfactant and increasing lung permeability
  • 20.  Recent work by Barie and colleagues demonstrates that free fatty acids are bound rapidly by albumin and transported through the bloodstream and lymphatic channels in this benign form.
  • 21. Obstructive theory A chemical mediator at the site of fracture releases mediators that affect solubility of lipids results in coalition and subsequent embolisation.
  • 22. What is the effect of along bone fracture An abundance of tissue thromboplastin is released with the marrow elements after long-bone fracture
  • 23. Intravascular coagulation by-products such as fibrin and fibrin degradation products then are produced complement system tissue thromboplastin
  • 24.  These blood elements, along with leukocytes, platelets, and fat globules, combine to increase pulmonary vascular permeability, both by their direct actions on the endothelial lining and through the release of numerous vasoactive substances.  In addition, these same substances activate platelet aggregation.
  • 25. Clinical Findings  most common etiologic factor –  -a high-energy Trauma to long bone or pelvis, including orthopedic  2nd or 3rd decade of life  or in a patient in the 6th-7th decade of life, when low-energy fractures of the hip are frequent.
  • 26. Physical:  Cardiopulmonary  Early persistent tachycardia  Patients become febrile with high-spiking temperatures  Patients become tachypneic, dyspneic, and hypoxic due to ventilation-perfusion abnormalities 12-72 hours after injury.
  • 27.  Subconjunctival and oral hemorrhages and petechiae also appear.
  • 28. Dermatologic • Alert clinicians may notice reddish-brown nonpalpable petechiae developing over the upper body, particularly in •only 20-50% of patients and resolve quickly • virtually diagnostic virtually diagnostic •axillae, within 24-36 hours of insult or injury.
  • 29.  Neurologic  Central nervous system dysfunction initially manifests as agitated delirium but may progress to stupor, seizures,  or coma and frequently is unresponsive to correction of hypoxia.  Retinal hemorrhages with intra-arterial fat globules are visible upon funduscopic examination.
  • 30. Signs  Raise in temprature (39-40deg C)  Tachypnea 30min or higher  Tachycardia-- > 140min or higher, BP is usually WNL  Long tract signs extensor posturing and deceribrate rigidity  Urinary incontinencehealthy patient with long bone # showing urinary incontinence needs to be ruled out for FES
  • 31. Sub clinical Nonfulminant subacute Fulminant types
  • 32. Sub clinical  Onset after injury 12-72 hrs  Mortality rate 0 %  Clinical presentation - nonspecific or absent symptoms moderate hypoxemia(Pao2 <80mm Hg in room air) moderate hypocapnia (Paco2<=30 mm Hg during spontaneous breathing) moderate decrease of platelet count (<200,000 micro L)
  • 33. Nonfulminant subacute  Onset after injury 12-96 hrs  Mortality rate 0 -5%  Clinical presentation dyspnea, tachypnea ,fever, tachycardia , petechiae cerebral signs hypoxemia (Pao2 <60mm Hg in room air) anemia thrombocytopenia and coagulation abnormalities lung opacities on chest radiograph
  • 34. Fulminant types  Onset after injury few hrs  Mortality rate >50%  Clinical presentation frank pulmonary edema moderate to severe hypotension cerebral signs severe hypoxemia and acidosis
  • 35. Management of Fat Embolism Lab.Findings & Radiographic evaluation. Treatment
  • 36. Lab. Findings 1. 1.ABGa)Hypoxemia(pO2<60mm Hg). 2. b) Acidosis(pH<7.3). 3. 2.HAEMATOLOGY- 4. a)Hb-low. b)Platelets- low 5. C) 6. d)PT/PTTK-high 7. e)ESR-elevated.
  • 37. Biochemistry  1.Fat macroglobinemia  2.Urine & Sputum fat globules.  3.Serum FFA’s-Increased.  4.Hypocalcemia(relative).  5.Levels of Cortisol,Glucagon & Catecholamines increase in proportion to the stress response to injury.
  • 38. ECG  Right axis deviation.  S-waves in lead –II.  Q-waves in lead –III.  ST-segment changes.
  • 39. Radiographic Evaluation  CHEST X-RAY-initially appears normal.  Dysnea  -within 72 hours diffuse B/L infilterates(SNOWSTORM appearance)  s/o—ARDS. SNOWSTORM
  • 40.  CT-HEAD-Cerebral edema & Haemorrhagic infarcts in white matter may be seen.
  • 41. Diagnosing FES Gurd‘criteria  one sign from major and at least  four signs from the minor criteria category
  • 42. Gurd major‘criteria  petechiae in a “vest” distribution  hypoxia, with a PaO 2 less than 60 mm Hg  pulmonary edema  cerebral manifestations.
  • 43. Gurd‘minor criteria  tachycardia, with a heart rate greater than 110 beats/minute  pyrexia, with a temperature higher than 103° F (39.4° C)  retinal changes  fat in urine or sputum  an unexplained drop in hematocrit or platelet count  an increasing erythrocyte sedimentation rate  jaundice  renal changes.
  • 44. TREATMENT 3 CORNERSTONES OF TREATMENT
  • 45. RESPIRATORY SUPPORT  Ranges from O2 admn to full resp. support with mechanical ventilation.  On pulse oximetry—  a)If PaO2<90mm=ABG analysis.  b)If PaO2 b/w 60-90mm=O2 by mask,  serial ABGs,  wait &watch for any deterioration.  c)If PaO2<60mm=INTUBATE & VENTILATE. PEEP if required.
  • 46. TREATMENT OF SHOCK SEVERITY OF FAT EMBOL. IS DIRECTLY PROPORTIONAL TO DEGREE OF SHOCK.
  • 47. ADDITIONAL THERAPIES  1)STEROIDS-  -they also decrease inflam.reaction in lungs caused by FFAs.  Decrease capillary leakage by stabilizing lysosomal & capillary membranes.  Prophyllactic dose of Methyl Pred.in high risk patients=10mg/kg body wt./q8h i.v(in 100ml saline).
  • 48.  2)ALCOHOL-Decreases ser. Lipase activity,limits lipolysis of fat & decr.FFAs  3)APROTININ-Protease inhibitor.Decr. Plat. Aggreg.& serotonin release.Decr. Incidence of fat emb. From 15% to 5%.  4)HYPERTONIC GLUCOSE-Metabol. Decreases production of FFAs.  .
  • 49. TIMING OF # STABILIZATION RIGID EARLY IMMOBILIZATION.  Seibel et al-10 days of skeletal traction of fracture femur with respect to early definitive # treatment-  a) x2 duration of ventilatory failure.  b) x4 no. of fracture complications.  c) x10 no. of positive blood cultures.
  • 50. TYPE OF STABILIZATION Reamed v/s Unreamed Femoral nailing. Pape et al-In patients with thoracic injury reaming has high rates of ARDS(33% v/s 8% for unreamed). Many studies disproove/attempt to disproove it. So it is INCONCLUSIVE/DEBATABLE.